The most significant findings in this study were that an individual’s initial level of joint ROM was not correlated with stretch-induced deficits and secondly, that four weeks of flexibility training did not diminish stretch-induced impairments. While there have been many studies demonstrating decreases in isometric force (Behm et al., 2001; Fowles et al., 2000; Kokkonen et al., 1998; Power et al., 2004), dynamic strength (Nelson and Kokkonen, 2001), and jump height (Young and Behm, 2003) following an acute bout of static stretching, there have been no studies reporting on the effect of greater joint ROM or flexibility training on stretch-induced impairments. Klinge et al., 1997 reported that the addition of flexibility exercises to a 13-week strength-training programme had no significant effect on the strength training responses. Wilson et al., 1992 found that the rebound bench press of powerlifters was enhanced following eight weeks of flexibility training due to an increased utilization of elastic strain energy during the lift. While Hunter and Marshall, 2002 demonstrated increases in countermovement jumps with 10 weeks of flexibility training, Guissard and Duchateau (1988) showed no change in MVIC torque or rate of torque development following 30 sessions of static stretching. However, none of the aforementioned studies involved an acute bout of stretching immediately prior to the post-training measures. It could be hypothesized that the repeated bouts of stretching associated with a flexibility-training programme would reduce impairments associated with a subsequent acute bout of static stretching. A more flexible musculotendinous unit (MTU) or a MTU that is more tolerant of stretch tension might accommodate the stresses associated with an acute bout of stretching more successfully than a stiff MTU. This was not the case in the present study. Since the stretching instructions were to stretch to the point of discomfort for both pre- and post-training, the intensity of stretching was relative to the stretch tolerance of the MTU. Whether an individual’s ROM was greater prior to training (correlation study) or became greater with training, the more flexible MTU would have been elongated to a greater extent during the acute bout of stretching than a less flexible MTU. Thus, irrespective of the bsolute change in ROM, it seems that the relative stretch-induced stress placed on the MTU leads to similar impairments. Although it was not incorporated in the present study, it is conceivable that if the absolute change in ROM used in the pre-training stretch intervention was matched post-training, the relatively less stress (smaller ROM) placed on the more flexible MTU would have resulted in less impairment. The decrements associated with the acute bouts of stretching both before and after the flexibility training programme reflect similar stretch-induced decreases in force (Behm et al., 2001; Fowles et al., 2000; Fowles and Sale, 1997), and power (Young and Behm, 2003) reported in other published studies. An acute bout of stretching has been reported to alter the length and stiffness of the affected limb MTU. Although the exact mechanisms responsible for increases in ROM following stretching are debatable, the increase has been attributed to decreased MTU stiffness (Wilson et al., 1991; 1992) as well as increased tolerance to stretch (Magnusson et al., 1996b). Studies have reported both decreases (Magnusson et al., 1996a; Toft et al., 1989) and no change (Magnusson et al., 2000) in MTU passive resistance or stiffness with an acute bout of stretching. Changes in MTU stiffness might be expected to impact the transmission of forces, the rate of force transmission and the rate at which changes in muscle length or tension are detected. A slacker parallel and series elastic component could increase the electromechanical delay by slowing the period between myofilament crossbridge kinetics and the exertion of tension by the MTU on the skeletal system. A lengthened muscle due to an acute bout of stretching could have a less than optimal cross-bridge overlap which, according to the length tension relationship (Rassier et al., 1999), could diminish muscle force output. The elongation of tendinous tissues can also have an effect on force output (Kawakami et al., 2002). Another possibility is that stretch-induced stress could have a detrimental effect of on neuromuscular activation (Avela et al., 1999; Behm et al., 2001, Power et al., 2004). Avela et al., 1999 investigated the effects of passive stretching of the triceps surae muscle on reflex sensitivity. Following one hour of stretching there were significant decreases in MVC (23.2%), EMG (19.9%), stretch reflex peak-to-peak amplitude (84.8%), and the ratio of H-reflex to muscle compound action potential (M-wave) (43.8%). Although neural propagation seemed unaffected (M-wave), afferent excitation of the motoneuron pool (H-reflex) was impaired. Although, Guissard et al., 2001 reported decreases in H-reflex excitability during passive stretching, the decrement was limited to the duration of stretching. Avela et al., 1999 suggested that the decrease in the excitation of the motoneuron pool resulted from a reduction in excitatory drive from the Ia afferents onto the -motoneurons, possibly due to decreased resting discharge of the muscle spindles via increased compliance of the MTU. Nonetheless, whether stretch- induced impairments arise from changes in muscle compliance solely or in concert with the afferent inhibition of the motoneuron, an increased ROM in the present study did not ameliorate the stretch- induced deficits. There were significant increases in active ROM associated with the flexibility-training programme (sit and reach: 11.8%, p < 0.01; hip extension: 19.7%, p < 0. 01 and hip flexion: 13.4%; p < 0.01). While the present study incorporated 20 sessions of stretching, others have reported statistically significant increases in ROM with only 12 stretches over a 4-week period (Davis et al., 2005). Since active stretches are limited by the strength of the opposing muscle groups, the increases in ROM may not be identical to passive flexibility measurements. However considering that activities of daily living almost never involve passive ROM, the active flexibility measures should better reflect daily realities. Not all power measures demonstrated stretch-induced decrements. While the countermovement jump height was diminished by an acute bout of stretching, drop jump height was not significantly affected. Both types of jumps were included in the flexibility training study since the 30 cm drop jumps emphasized a short contact time (typically under 200 ms) whereas the countermovement jump typically had a greater duration (could not be directly measured in the present study) of the stretch-shortening cycle. It was felt that the short contact time drop jumps would mimic actions such as sprinting whereas the countermovement jump would be more typical of power movements such as shot put, basketball jumps, skating and other activities involving force exerted over a longer duration. Deficits with countermovement jumps demonstrated that static stretching held to the point of discomfort would adversely affect the aforementioned type activities. A lack of change in drop jump height could be attributed to the significant stretch- induced increase in drop jump contact time (pre-training: 5.4% and post-training: 7.4%). Increases in drop jump contact time post- acute stretching would allow for a greater impulse (force x time) to be exerted possibly permitting stretch-induced diminished forces (as exemplified by the decreased MVIC and countermovement jump) to be exerted over a longer duration. The modest number of participants and the use of only men might hamper the implications and applications of the longitudinal study. Nonetheless, the participation of men only should not significantly affect the external validity of the findings, as the stretch-induced deficits in force with the cross-sectional study (men and women) were very similar to the training study (men) and other comparable studies (Behm et al., 2001; 2004; Fowles et al., 2000; Power et al., 2004). Furthermore, since the data was normally distributed and most effect sizes were moderate, an argument can be made for the assumption of external validity. |